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Wednesday, January 23, 2013

Are starches safe? Part 2

(SEM image of corn-derived granule in blood after a serving of mueseli)

Previously on this blog, it was
stated that starches and cereal grains were good food for cows and horses, but not man.
Man is instead better off eating food that is readily, easily, and perfectly digested. Cases in point: fruit and fruit juices.I will put forth herein why this is the case,
and expand on some of the perils of excess starch consumption discussed in
the last post.

A prominent feature of consuming starches concerns the
previously discussed phenomenon called persorption (aka translocation).Briefly, persorption describes the absorption
of non-soluble microparticles through the intestinal lining and thereafter into
the lymph vessels, mesenteric veins, and then distributed to tissues throughout the body.

Although persorption was known about since the mid
19th century, the research on it has been sparse. (On my last search
for articles on the topic in pubmed and medline, using the search terms
“persorption” and “starch granule”, only five results were found.)

Nonetheless, there is still a lot we do know.For one, we know that starch granules can
appear, really, anywhere in the body, including the urine, cerebrospinal fluid,
peritoneal fluid, fetal blood, umbilical cord, and milk of lactating mothers.

Two, we know that the indigestible parts of plants
are the main sources of particles for persorption processes, namely starch
granules, and the smaller they are – like the granules found in corn, wheat,
and oats – the more likely they are to undergo persorption processes.

Three, we know that stress, physical injury,
toxins, and inflammation can increase the persorption rate considerably by
disrupting the tight junctions between enterocytes, which normally keep
persorption processes in check.

Four, we know – because it’s been confirmed by way
of electron microscopy – that starch granules appear in the blood on oral
consumption of a variety of starchy foods without a doubt.And, electron microscopy has confirmed what
researchers decades before meticulously counted out – that starch granules are
found on the order of 10-100 granules per 100 milliliters of blood, depending
on the starch source, inherent variations among people, drug use, etc.

And five, we know that these microparticles are
detected in the body as soon as 2 minutes after consuming them, reaching peak
concentrations at around 12 hours, before being completely eliminated from the
body by 24.

An area of research that is worthy of further
investigation is the fate and bodily effects of these microparticles once they
are persorbed into the body.Though,
it’s at least known that larger granules clog arterioles, and that the
consumption of the aforementioned starches are provisionally linked to
autoimmune diabetes (Mueller et al., 2009) and senile dementia (Freedman, 1991).

The chronic ingestion of starches could, sooner or
later, cause uncontrolled fermentative activity in the intestines with an attendant
production of gases, acids, and alcohol (Hamer, De Preter, Windey, & Verbeke, 2012).These byproducts of microbial fermentation
end up causing intestinal irritation and inflammation that in turn, compromise our ability to absorb nutrients properly – predisposing to more fermentative
activity.

Then due to insufficient nutrient assimilation,
the enteric nervous system weakens and this leads to an impairment of
digestion, again, compromising our ability to defend against fermentative processes even
further.

Easily digested foods are ideal and should form the
lion’s share of our diets.As compared
to starches, fruit is highly digestible – some fruit more than others – and are
thus much less liable to ferment.

Another feature of consuming starches is the rise
in lipopolysaccharide after meals. If
lipopolysaccharide levels increase 2- to 3-fold above normal, metabolic
endotoxemia manifests, where pathological processes – mediated by macrophages –
first produce inflammation and insulin resistance in the liver, and thereafter, in the adipose
tissue and muscles.

The mechanism by which LPS is absorbed at the
surface of the intestinal lining is different from persorption in that LPS is
absorbed by way of newly formed chylomicrons in the enterocytes, wherefrom they
– via chylomicron remnants – are taken up by the liver.This is why diets high in fats – that is,
long chain fats – consistently increase LPS concentrations in the body (and why
short chain fats don’t) and why the damages incurred from LPS first
manifest in the liver (Ghoshal, Witta, Zhong, De Villiers, & Eckhardt,
2009).

GF: germ-free
(Backhed, Manchester, Semenkovich, & Gordon, 2007)

I think the importance of LPS and bacterial fermentative processes is clearly illustrated by an experiment wherein mice reared without germs had about 60
percent less body fat than normal mice, even though the germ-free mice and
normal mice ate the same amount of food (and lost equal amounts of fat in their feces and absorbed an equal amount of fat) on switching to a so-called Western
diet, which was high in fat and sugar (41 percent of calories of each) for 8 weeks. The resistance to fattening in the germ-free mice was accounted for by an increase in their triglycerides and their energy expenditures.

Metabolic endotoxemia also promotes – in a vicious
cycle – the release of fatty acids, and these fatty acids (i.e., NEFA) in turn, stimulate their own uptake and oxidation, and thereafter, inhibit the use of
glucose, thereby initiating the stress metabolism. . . .

Nonetheless, fructose – of which starch contains
none of – is supportive in that it raises energy expenditure and carbohydrate
oxidation more than glucose does, about 1.5-fold more, and at the same time, stimulates insulin secretion about 4-fold less.Thus the increase in energy expenditure by fructose is not caused by
insulin alone.

But rather, other thermogenic mechanisms are involved
as well, as evidenced, for instance, by a 40 percent blunted increase in energy
expenditure when fructose was given with a β-blocker (Tappy et al., 1986).

Furthermore, because a high rate of glucose oxidation is required for fructose-induced thermogenesis to kick in, fructose permits (and could restore) glucose use (Ravussin, Acheson, Vernet, Danforth, & Jequier,
1984).

Thermogenesis can be simply represented by energy expended
in excess of the calories from, say, fructose or glucose ingested:

Δ energy expenditure (from baseline) / g carbohydrate ingested

Taken together, although obesity and diabetes are associated with
lower-than-normal rates of carbohydrate oxidation, diet-induced thermogenesis,
and excessive fat oxidation already, fructose can, to some extent, normalize the derangements associated with metabolic endotoxemia – without the need for pharmacological doses of insulin.

Fructose (and sucrose) is additionally supportive
in that it – more efficiently than glucose – stimulates the deiodination of
thyroid hormone to its active form, T3.Thus cells throughout the body see a greater
exposure to T3, permitting the long-term effects of T3, such
as the upregulation of enzymes that control basal thermogenesis (e.g., UCP) and
energy production (e.g., cytochrome c oxidase).

In summary, a cereal grain- and starch-based diet could lead to degenerative changes in the bowels that are self-reinforcing, whereby damages sustained in the digestive tract
predispose to further fermentative processes – precisely what initiated the
damages in the first place.Consequences
include metabolic endotoxemia and persorption with an attendant slowing of the
metabolic rate, loss in energetic efficiency, and a switch to predominantly fat
oxidation.

Fructose, however, through various mechanisms –
like insulin – can help to soften these metabolic derangements.

Eradicating foods that are resistant to digestion
in the upper intestines curtails fermentative activity in the lower intestines
and thus, prevents damages that permit substances like starch granules to
pass through at a high rate.The production
of LPS is blunted, too, simply by virtue of keeping bacterial proliferation in
the intestines in check. Consequently, the long-term sequelae seen in the
digestive tract in investigations made during the 19th century can
be, at the very least, delayed.

Some degree of bacterial fermentation is
physiological and could even be beneficial.However, as evidenced in the germ-free rodents, it is not absolutely
essential for life – albeit in artificial settings.Nonetheless, even fully digestible foods
provide fodder, in small amounts, to keep intestinal bacteria adequately fed so
to speak.

5 comments:

In the university residence that I'm currently staying, high quality, ripe fruit is very difficult to find. All we get is oranges, bananas, and apples - all non-organic, and barely ripe. When I eat an orange, I get constipated; when I eat an apple, I see apple shreds in my feces, and bananas make me crazy bloated whether ripe or unripe. Good quality fruits on the other hand, seem to be digested a little better, but I still get very bloated about 1 hour of eating them (same with pretty much any food, actually). My blood sugar is better off with fruits, but as I said, it's difficult to find organic, ripe peaches or grapes here. Out of salted rice, wheat bread, breakfast cereal, and gluten free bread (made with potato starch etc), which would be the least damaging? Due to my IBS, I tried so many different diets in the past, but I really don't feel much difference. Perhaps it's because I wasn't able to stick with them long enough. p.s. Maybe you should add "about me" page on your blog. I'm sure readers would be interested.

Hey Steph. Do you have access to orange juice or grape juice? Concentrates are okay, if that's all you can get.

Salted rice is the best by far. Just make sure it's cooked well -- even better is if you overcook it.Create a diet centered on soft, gentle, and fully digestible foods. So, milk, yogurt, fruit juices, well-ripened vegetables like cucumbers and tomatoes, stews and soups, and keep the starches and cereal grains to a minimum. Overgrowth in the bowels causes IBS, so antibiotics and laxatives can be supportive, too.

Thanks for the suggestion, I'll get to putting up an about me page as soon as I can.

very interesting post, and in the main I think you're spot on... but why advocate antibiotics? I've seen this argument before in regard to eliminating SIBO but not seen it work. One friend of mine who had antibiotic treatment for bacterial overgrowth found that her SigA levels plummeted and then other strains of commensal and/or pathogenic bacteria and yeasts that hadn't been there before started to appear. In my own experience it took me years to get my gut health better through a change in dietary regime, use of HcL, etc and then since having my son and being in hospital for 10 days because of a haemorrhage and infection, having to take endless rounds of IV and oral antibiotics, my gut has gone back to a horrible fermenting mess. I now can't tolerate anything fibrous, none of the cruciferous veg etc, all things I could happily eat before. Surely antibiotics just allows the gut flora to completely alter, and not for the good??

Andrew what are your views on gingivitis/gum disease?, i can't really eat sugar because my gums recede every time when i do. I also have high blood sugar, my doctor said pre-diabetes, so how could i do this diet without sugar?. I can drink milk but that is about the only thing with sugar in it that doesn't get my teeth/gums.